ABSTRACT
Background and aims: There´s emerging evidence on the association of GBS with SARS-CoV-2 infection. Neurotropism by coronavirus has been documented as well as various neurological manifestations such as encephalitis, stroke, encephalopathy and peripheral nerve disease. Methods: A 67-year-old male, no comorbidities presents three weeks prior to admission with fever, cough, taste and smell disturbances, myalgias, asthenia, clumsy hand movements and progressive lower limbs weakness. 15 days prior to admission: difficulty swallowing, diaphoresis. At admission: breathing difficulty and palpitations. Glasgow 13 E4 V5 M4, bulbar compromise, bradylalia, diminished gag reflex, sternocleidomastoid and trapezius weakness, MRC scale upper and lower limbs: proximal 3/5 distal 2/5, generalized areflexia, distal diffuse hypoesthesia Results: Ferritin 519 LDH 236 D Dimer >10,000 Hgb 19 WBC 11590 L 12% N 80% P 241,000 CK 111 CK MB 17. Chest CT: COVID19 pneumonia, CO-RADS 3. Pulmonary angiography: Posterior right lower lobe segmental PE. Scores: PESI 108, Geneva 10. SARS-CoV-2 PCR negative, SARS-CoV-2 IgG/IgM: Positive. Lumbar puncture not performed due to PE. Met Asbury GBS criteria, HUGHES 4, mEGOS 8 at admission, EGRIS 4. Progression of ascending symmetrical bilateral flaccidity with respiratory failure requiring mechanical ventilation for 10 days, tracheostomy and gastrostomy were performed. Discharged at day 60 with muscle strength recovery, upper limbs 4/5 and lower limbs 3/5, Sensitivity recovery, diminished lower limb reflexes. Therapy: Enoxaparin 60mg every 12h, Immunoglobulin 0.4mg/kg/day/5 doses. Discharge HUGHES 3. [Formula presented] [Formula presented] Conclusions: GBS is caused by an anomalous response of the immune system to an infectious agent. This particular patient presents with a GBS associated with SARS-CoV-2 infection and PE.